David T Lawrence, Stephen G Dobmeier, Laura K Bechtel, Christopher P Holstege
Food poisoning.
Emerg Med Clin North Am. 2007 May;25(2):357-73; abstract ix. doi: 10.1016/j.emc.2007.02.014.
Abstract/Text
Food poisoning is encountered throughout the world. Many of the toxins responsible for specific food poisoning syndromes are no longer limited to isolated geographic locations. With increased travel and the ease of transporting food products, it is likely that a patient may present to any emergency department with the clinical effects of food poisoning. Recognizing specific food poisoning syndromes allows emergency health care providers not only to initiate appropriate treatment rapidly but also to notify health departments early and thereby prevent further poisoning cases. This article reviews several potential food-borne poisons and describes each agent's mechanism of toxicity, expected clinical presentation, and currently accepted treatment.
Abstract/Text
Following nerve injury, primary sensory neurons (dorsal root ganglion [DRG] neurons, trigeminal neurons) exhibit a variety of electrophysiological abnormalities, including increased baseline sensitivity and/or hyperexcitability, which can lead to abnormal burst activity that underlies pain, but the molecular basis for these changes has not been fully understood. Over the past several years, it has become clear that nearly a dozen distinct sodium channels are encoded by different genes and that at least six of these (including at least three distinct DRG- and trigeminal neuron-specific sodium channels) are expressed in primary sensory neurons. The deployment of different types of sodium channels in different types of DRG neurons endows them with different physiological properties. Dramatic changes in sodium channel expression, including downregulation of the SNS/PN3 and NaN sodium channel genes and upregulation of previously silent type III sodium channel gene, occur in DRG neurons following axonal transection. These changes in sodium channel gene expression are accompanied by a reduction in tetrodotoxin (TTX)-resistant sodium currents and by the emergence of a TTX-sensitive sodium current which recovers from inactivation (reprimes) four times more rapidly than the channels in normal DRG neurons. These changes in sodium channel expression poise DRG neurons to fire spontaneously or at inappropriately high frequencies. Changes in sodium channel gene expression also occur in experimental models of inflammatory pain. These observations indicate that abnormal sodium channel expression can contribute to the molecular pathophysiology of pain. They further suggest that selective blockade of particular subtypes of sodium channels may provide new, pharmacological approaches to treatment of disease involving hyperexcitability of primary sensory neurons.
Copyright 1999 John Wiley & Sons, Inc.
Abstract/Text
Between 1989 and 1999, 25 cases of puffer fish poisoning (PFP) were admitted to the medical service of Chon Buri Hospital. The severity of the poisoning was classified into four stages based on clinical signs and symptoms of PFP. Of the 25 patients, 23 were males and 2 were females. Three patients were in stage 1, four were in stage 2 and eighteen were in stage 4. Paresthesia was the early presenting complaint of all patients. Paresthesia consisting of either numbness or tingling of lips, tongue, around the mouth, hands, and feet. Muscle weakness, dizziness, vertigo, nausea and vomiting were common complaints. Eighteen patients developed acute flaccid paralysis and respiratory failure requiring ventilatory support. All patients received symptomatic and supportive treatment and general supportive care, including gastric lavage and intravenous fluid. Intubation and mechanical ventilation was considered especially when paralysis was progressing rapidly. Most were taken off the respirator 12-48 hours later. All patients completely recovered without any sequelae. Clinical features of PFP, toxicity of puffer fish and management were discussed.
Abstract/Text
Puffer fish poisoning has been documented rarely in Australia. It results from ingesting tetrodoxtoxin found in the liver, ovaries, intestines and skin of the fish. Over a recent 16-month period, 11 cases of puffer fish poisoning were reported to the NSW Poisons Information Centre. Symptoms of poisoning may include paralysis, respiratory failure, numbness, paraesthesia, nausea and ataxia. Health professionals should be aware of the condition so as to institute early and appropriate management.
Chorng-Kuang How, Chii-Hwa Chern, Yin-Chieh Huang, Lee-Min Wang, Chen-Hsen Lee
Tetrodotoxin poisoning.
Am J Emerg Med. 2003 Jan;21(1):51-4. doi: 10.1053/ajem.2003.50008.
Abstract/Text
Tetrodotoxin (TTX) poisoning, although uncommon, is frequently seen in Taiwan, Japan, and Southeast Asia. It is rare but significant in the United States as well. Only three cases have been reported in the EM literature. We report an outbreak of six cases of TTX poisoning from eating puffer fish. On April 17, 2001, an outbreak of TTX poisoning occurred among Mainland Chinese fishermen who shared puffer fish on their boat in the Taiwan Strait. All six cases were middle-aged men (aged 32-49 yr). Onset of symptoms began approximately 2 to 3 hours after ingestion; symptoms included orolingual numbness, acroparesthesia, and breathlessness. As a result of delayed transportation and initial resuscitation, one patient presented in full cardiac arrest, with recovery of spontaneous circulation after successful cardiopulmonary resuscitation. With the exception of this patient, the initial acid-base abnormalities were inconsistent with severity of illness and mild hypercapnia was common (4 out of 5). The patient who presented in full arrest died 1 day after admission as a result of intractable bradycardia (complete atrioventricular block), a finding rarely mentioned in the literature, despite intravenous atropine and dopamine infusion. The remaining patients survived without significant sequelae and were discharged after short-term observation and supportive care, although some had neurologic and cardiopulmonary manifestations (muscle weakness, hypotension, hypoxemia, and hypercapnia). Some mildly hypoventilated patients recovered well without endotracheal intubation and ventilatory support. Favorable outcomes in most patients can be obtained if aggressive supportive treatment is provided in time. Thus, appropriate prehospital and ED ventilatory support (the implementation of a bag-valve mask or endotracheal intubation with good ventilatory support) is mandatory for those patients with respiratory failure. Most patients experience onset of symptoms within 6 hours of ingestion, but a few have a delayed onset up to 20 hours. Therefore, for those TTX-intoxicated patients without immediate prominent respiratory insufficiency, at least 24 hours of intensive monitoring of their respiratory state is necessary because of the different susceptibility and unpredictability of an individual course.
Copyright 2003, Elsevier Science (USA). All rights reserved.)
